Stress Doppler echocardiography for identification of susceptibility to high altitude pulmonary edema
Ekkehard Grünig, MD*,
Derliz Mereles, MD*,
Wulf Hildebrandt, MD ,
Erik R. Swenson, MD ,
Wolfgang Kübler, MD*,
Helmut Kuecherer, MD* and
Peter Bärtsch, MD
* Department of Cardiology, University of Heidelberg, Heidelberg, Germany
Institute of Sports Medicine, University of Heidelberg, Heidelberg, Germany

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Figure 1 PASP response to prolonged hypoxia. Discrimination between controls and HAPE-S subjects by their PASP response to hypoxia estimated by Doppler-echocardiography. HAPE-S, subjects susceptible to high altitude pulmonary edema (n = 9); CONTROLS, control subjects (n = 11). The study was discontinued at 55 min of hypoxia in one control subject. No significant differences at rest between both groups (p = 0.36). *PASP in HAPE-S subjects compared with control subjects at 45 (p = 0.0012), 90 (p = 0.0016) and 240 (p < 0.02) min of hypoxia.
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Figure 2 Time course of PASP changes during supine bicycle exercise. Discrimination between HAPE-S vs. control subjects at 50 (p = 0.24), 75 *(p = 0.03), 100 **(p = 0.06) and 125 W ***(p = 0.06).
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Figure 3 PASP response to exercise. Discrimination between controls and HAPE-S subjects by their PASP response to exercise estimated by Doppler echocardiography. HAPE-S, subjects susceptible to high-altitude pulmonary edema (n = 9), CONTROLS, control subjects (n = 11). No significant differences at rest between both groups (p = 0.28). *Mean maximal PASP in controls (36 ± 3 mm Hg) vs. HAPE-S (55 ± 11 mm Hg) subjects, p < 0.002.
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Figure 4 Impaired LV relaxation in HAPE-S subjects during exercise and prolonged hypoxia assessed from mitral inflow velocities. Both exercise and prolonged hypoxia decreased E/A ratios to levels < 1.0 in six of nine patients susceptible to HAPE but in only one control patient; *p = 0.01 at peak exercise, and at **45, ***90 and ****240 min of hypoxia.
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